Thyroid status in chronic phase chronic myeloid leukemia patient treated with Tyrosine Kinase Inhibitor

Abstract

Background
Thyroid dysfunction is a recognized side effect of Tyrosine Kinase Inhibitor (TKI) therapy in chronic myeloid leukemia (CML), most commonly hypothyroidism, characterized by elevated thyroid-stimulating hormone and reduced free thyroxine levels.


Objective
To evaluate thyroid status with chronic phase CML managed with TKI.


Patients and methods
This prospective cross-sectional hospital-based research has been done at the Clinical Hematology Unit, Internal Medicine Department, at Assiut University Hospital. It has been done in the duration between 2023 and 2024.


Results

Baseline characteristics were similar except higher age in no major molecular response (no-MMR) (67.1 vs. 56.5 years;
P
=0.001). Most patients were male; the Charlson index and comorbidities were comparable. In MMR, 2 had subclinical hypothyroidism initially, 2 developed autoimmune hypothyroidism at 6 months; one no-MMR had subclinical hypothyroidism. Anti-thyroid peroxidase (anti-TPO) was higher in MMR at 6 months (30.6 vs. 18.1 IU/ml;
P
=0.04), and thyroid-stimulating hormone and anti-TPO increased for all TKIs; breakpoint cluster region and Abelson murine leukemia viral oncogene homolog 1 declined significantly within each group, with no between-group difference.



Conclusion
This study shows that inflammatory, metabolic, and immunological parameters can predict early molecular response in CML cases on TKI therapy, with elevated NLR, PLR, and TG/HDL ratio as significant negative predictors of achieving MMR at 6 months, while subclinical thyroid autoimmunity, especially elevated anti-TPO antibodies, is associated with a favorable TKI response.